Publication Type:Journal Article
Source:Kidney Int, Volume 90, Issue 6, p.1146-1148 (2016)
A new study by Kuwagata et al. now shows that aberrant activation of the mechanistic target of rapamycin complex 1 in renal tubular cells causes their injury and cell death by enhancing endoplasmic reticulum stress and cell death pathway under diabetic conditions. The study has revealed a novel molecular mechanism in which mechanistic target of rapamycin complex 1 stimulates the tumor necrosis factor signaling by attenuating miR-148b-3p, thereby deteriorating renal tubular cell dysfunction under diabetic conditions.